35822-46-9Clc1cc2c(c(Cl)c1Cl)Oc1c(Cl)c(Cl)c(Cl)c(Cl)c1O2WCLNVRQZUKYVAI-UHFFFAOYSA-N1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin is an off-white powder. Insoluble in water. (NTP, 1992)
35822-46-9、37871-00-4Insoluble (NTP, 1992)
Water solubility= 1.9X10-3 mg/l (measured)
1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin is an off-white powder. Insoluble in water. (NTP, 1992)
Off-white solid; [CAMEO] White crystalline solid; [MSDSonline]
안전 정보는 참고용이며, 공급업체의 물질안전보건자료(SDS), 관련 법규 및 전문가 평가를 대체하지 않습니다.
Warning
H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]
P203, P261, P264+P265, P271, P273, P280, P304+P340, P305+P351+P338, P318, P319, P337+P317, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 39 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Hazard Traits - Bioaccumulation; Carcinogenicity; Dermatotoxicity; Endocrine Toxicity; Environmental Persistence; Environmental tox; Hematotoxicity; Hepatotoxicity and Digestive System Toxicity; Reproductive Toxicity; Respiratory Toxicity
Regulation (EC) No 178/2002 (amended)
Skene SA et al; Hum Toxicol 8 (3): 173-204 (1989). Polychlorinated Dibenzo-P-Dioxins and Polychlorinated Dibenzofurans: The Risk to Human Health. A Review.
WHO; Environ Health Criteria 88: Polychlorinated Dibenzo-p-dioxins and Dibenzofurans (1989)
The half-lives of 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin, 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin, and octachlorodibenzo-p-dioxin /were calculated/ to be about 3.5, 3.6 and 2 years, respectively. The estimation was based on the analysis of fat tissue biopsies collected with an interval of 28 months from one 14 year old girl who for a period of about 2-3 years had been exposed to technical pentachlorophenol.
The effects of subchronic octachlorodibenzo-p-dioxin exposure was examined in rats over a 13 wk period. Male Fischer 344 rats were treated with 50 ug/kg (14)C labeled octachlorodibenzo-p-dioxin by gavage for 10, 20, 40, or 65 doses (once per day 5 days per wk) and sacrificed 3 days postexposure. Hepatic accumulation was associated with alterations of several biochemical parameters. In animals treated 65 times, ethoxyresorufin-O-deethylase activity was elevated 40 fold over controls; total cytochrome p450 content doubled and exhibited a 2 nanometer blue shift in the Soret maximum for the reduced hemoprotein-CO complex. Cytochrome p450c and cytochrome p450d were significantly increased, while cytochrome p450b levels were unaltered. Nearly all the dioxin congeners present in liver were represented by octachlorodibenzo-p-dioxin, with a slight amount ofheptachlorinated dioxin present. It was concluded that subchronic octachlorodibenzo-p-dioxin exposure causes toxic effects similar to those observed with other dioxins, but with far less potency than 2,3,7,8-tetrachlorodibenzo-p-dioxin. /Octachlorodibenzo-p-dioxin/
CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (L177)
After 21 daily doses of 100 ug octachlorodibenzo-p-dioxin containing 12.6 picograms (35)S-thio-heptachlorodibenzo-p-dioxin to male Sprague-Dawley rats, the radioactivity was mainly recovered in the feces and urine, the percentages of the ingested radioactive doses being 93 (+ or - 6) and 5.2 (+ or - 0.8)% respectively. The high fecal excretion suggests poor absorption. Of the radioactive body burden, 50% was contained in the liver. The microsomal fractioncontained 96.3 (+ or - 8.2)% of the hepatic radioactivity.
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DTXSID1052034CHEBI:81505NRCC; Polychlorinated Dibenzo-p-dioxins: Limitations to the Current Analytical Techniques, Publication NRCC No 18576 (1981). A technical review and assessment of the methodology for the analysis of polychlorinated dibenzo-p-dioxins in a variety of substrates. Analytical methodology was evaluated and safety procedures were suggested.
Olson JR et al; Chemosphere 18 (1/6): 371-81 (1989). A review of the toxicological and pharmacokinetic literature on chlorinated dibenzo-p-dioxins and dibenzofurans was presented to evaluate the accuracy and currency of established toxicity equivalence factors. /Chlorinated dibenzo-p-dioxins/
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.
SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then dampen the solid spill material with toluene, then transfer the dampened material to a suitable container. Use absorbent paper dampened with toluene to pick up any remaining material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent-wash all contaminated surfaces with toluene followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.
0.013 [mg/m3]
0.14 [mg/m3]
0.85 [mg/m3]
1,2,3,4,6,7,9-Heptachlorodibenzo-p-dioxin was found at concn ranging from 1.6 to 580 parts/trillion (whole, wet weight basis) in 46 adipose tissue samples collected in 1976 from the general Canadian adult population; all of the samples contained the compound and the mean concn was 135 parts/trillion(1). Concn of 1,2,3,4,6,7,9- and 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin ranged from not detected to 5.3 and from 39.4 to 119 parts/trillion, respectively, in 5 sc tissue samples taken in 1983-1984 from the Binghamton, NY, general population; the concn of the two isomers were 9.6 and 209 parts/trillion, respectively, in sc tissue samples from one Binghamton, NY, State Office Building worker exposed following the 1981 PCB transformer fire(1). The avg total heptachlorodibenzo-p-dioxin concn in human adipose tissue were 97 parts/trillion in 31 samples taken in Sweden in 1982-83, 137 parts/trillion in 13 samples taken in Canada in 1976, 116 parts/trillion in 46 samples taken in Canada in 1980, and 164 parts/trillion in 8 samples taken in the U.S. in 1982-83(2). The avg total concn in the fat fraction of human milk were 59.5 picogram/g in 4 samples from Sweden, 72.8 picogram/g in 5 samples from Germany, and 174 picogram/g in 1 sample from Denmark(2).
Heptachlorodibenzo-p-dioxin was detected at concn of 8.5 and 89 parts/trillion (wet weight and lipid basis, respectively) in one of 9 samples human breast milk taken from South Vietnam in 1973; the compound was not detected in the other 8 samples (detection limit 2 parts/trillion(1). The concn in breast milk taken from 2 of 3 U.S. women in the 1970s ranged from 1.7 to 2.5 parts/trillion (wet weight basis) and 44 to 61 parts/trillion (lipid basis)(1). The 1,2,3,4,6,7,8-isomer was found in 9 of 11 samples of human milk collected in South Vietnam in 1985 at concn in the positive samples ranging from 19 to 172 parts/trillion (lipid basis) (detection limit generally between 0.1 and 0.2 parts/trillion); two of the samples were composites of three samples and one was a composite of 4 samples(1). The 1,2,3,4,6,7,8-isomer was found in 2 samples of human breast milk collected in 1986 in Binghamton, NY, at concn of 1.26 and 1.74 parts/trillion (wet weight basis) and 44 and 60 parts/trillion (lipid basis)(1). The concn of 1,2,3,4,7,8,9-heptachlorodibenzo-p-dioxin in composite samples of human adipose tissue as measured in the EPA fiscal year 1982 National Human Adipose Tissue Survey (NHATS) ranged from not detected (detection limit 23 picogram/g) to 390 picogram/g and the avg concn was 87 pg/g; the average concn was approximately 140, 80, and 42 picogram/g in samples from individuals >45 years old, 15-44 years old, and 0-14 years old, respectively(2).
The total concn of heptachlorodibenzo-p-dioxin in tissue from 28 adults from the Munich, Germany, area ranged from 35.1-246 parts/trillion (avg 106.7 parts/trillion) in adipose tissue and 95.7-3463.1 parts/trillion (avg 1002.4 parts/trillion) in liver tissue; the concn of heptachlorodibenzo-p-dioxin in adipose tissue from 8 infants ranged from 11.8-51.1 parts/trillion (avg 27.1 parts/trillion)(1). Pool samples of human milk in 1988 from Birmingham and Glasgow, UK, (40 mothers each city) contained 76 and 65 parts/trillion 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (fat basis), respectively(2). The concn found in a WHO/EURO Interlaboratory Comparison of a pooled 1987 sample of European human milk from a number of mothers and locations that were not specified contained 46 parts/trillion (fat basis)(2). The 1,2,3,4,6,7,9-isomer was detected in samples of adipose tissue collected in 1985 from 9 of 13 Japanese cancer patients at concn ranging from 14-53 picogram/g (wet weight basis; 28 picogram/g avg concn); the 1,2,3,4,6,7,8-isomer was found in 12 of the 13 samples at concn ranging from 29-180 pg/g (77 picogram/g avg) (detection limits not specified)(3).
The range of avg concn of total heptachlorodibenzo-p-dioxin found in many of the studies of human adipose tissue from various industrial countries (excluding China and the north of Vietnam) is 87-230 parts/trillion(1).
Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (L177, L178)
TERRESTRIAL FATE: If heptachlorodibenzo-p-dioxin is released to soil, it will be expected to be immobile based upon an estimated Koc of 7.8X10+5 which can be calculated(SRC) from a measured water solubility of 1.9X10-3 mg/l(2) using a recommended regression equation(1,SRC). It should not, therefore, leach through soil(3). It will not hydrolyze in soil(1). Based solely upon an estimated Henry's Law constant of 2.18X10-5 atm-cu m/mole(4,SRC), volatilization from near-surface soil may be expected to be significant(SRC). However, strong adsorption to soil is expected to greatly attenuate the rate of volatilization from near-surface soil(SRC). It is not known whether heptachlorodibenzo-p-dioxin biodegrades in soil(SRC).
AQUATIC FATE: If heptachlorodibenzo-p-dioxin is released to water, it will be expected to strongly adsorb to sediment and suspended particulate matter based upon an estimated Koc of 7.8X10+5 which can be calculated(SRC) from a measured water solubility of 1.9X10-3 mg/l(2) using a recommended regression equation(1,SRC). Bioconcentration in aquatic organisms may be important based upon measured BCF ranging between 89.1-1700(3-5). It may be susceptible to direct photolysis in near-surface surface water based upon the adsorption of light at wavelengths >290 nm exhibited by other polychlorodibenzo-p-dioxins including hexachloro- and octachlorodibenzo-p-dioxins(6). Hydrolysis is not expected to be important(1). It is not known whether heptachlorodibenzo-p-dioxin biodegrades in water under environmental or laboratory screening test conditions. The half-life for volatilization of heptachlorodibenzo-p-dioxin from a river one meter deep flowing 1 m/sec with a wind velocity of 3 m/sec is estimated to be 3.7 days at 25 °C(1) based on an estimated Henry's Law constant of 2.18X10-5 atm-cu m/mole(7,SRC). Strong adsorption to sediment and suspended particulate matter, however, is expected to greatly attenuate the rate of volatilization in many natural waters(SRC). A half-life of >51 years for volatilization from a model pond can be estimated using a three-compartment EXAMS model which considers the effect of adsorption(8,SRC).
ATMOSPHERIC FATE: If heptachlorodibenzo-p-dioxin is released to the atmosphere, it can be expected to exist both in the vapor and particulate phases in ambient air(1,SRC) based upon an estimated vapor pressure of 7.4X10-8 mm Hg calculated(SRC) from a measured water solubility of 1.9X10-3 mg/l at 25 °C(2) and an estimated Henry's Law constant of 2.18X10-5 atm-cu m/mole at 25 °C(3,SRC). It has been estimated that polychlorodibenzo-p-dioxins such as heptachlorodibenzo-p-dioxin are likely to be associated with air particulate matter(4). The rate constant for the vapor phase reaction of heptachlorodibenzo-p-dioxin with photochemically produced hydroxyl radicals has been estimated to be 1.3X10-12 cu cm/molecule-sec at 25 °C(4,SRC) which corresponds to an atmospheric half-life of 12.3 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(SRC). Heptachlorodibenzo-p-dioxin may be susceptible to direct photolysis in the atmosphere and in near-surface surface water based upon the adsorption of light at wavelengths >290 nm exhibited by other polychlorodibenzo-p-dioxins including several hexachloro- isomers and octachlorodibenzo-p-dioxin(5).
A survey of 25 composite samples from 10 food classes including meats, eggs, milk, fruits, and vegetables collected at an unspecified time in the US and Canada indicated that total concn of heptachlorodibenzo-p-dioxin was below detection limits (detection limits 1-4 parts/trillion) in plant derived foods and in all animal derived foods tested except in chicken samples from Quebec which contained a maximum concn of 15 parts/trillion (fresh weight basis)(1). The following concn (fat basis) were found in chicken eggs collected from farms and stores in March 1988 in the vicinity of a pentachlorophenol plant near Polermo, CA, at which a fire occurred in April 1987: Polermo (4.5 km south of facility), 157 pg/g; Oroville, CA advisory area (1.5 km southeast of facility), 443 pg/g; and general commercial eggs from facility in Oroville and local stores, 7.7 pg/g; chicken fat and liver concn in chickens from the advisory area contained 495 and 835 pg/g median concn(2).
Heptachlorodibenzo-p-dioxin was detected at concn of 8.5 and 89 parts/trillion (wet weight and lipid basis, respectively) in one of 9 samples of human breast milk taken from South Vietnam in 1973; the compound was not detected in the other 8 samples (detection limit 2 parts/trillion(1). The concn in breast milk taken from 2 of 3 U.S. women in the 1970s ranged from 1.7 to 2.5 parts/trillion (wet weight basis) and 44 to 61 parts/trillion (lipid basis)(1). The 1,2,3,4,6,7,8-isomer was found in 9 of 11 samples of human milk collected in South Vietnam in 1985 at concn in the positive samples ranging from 19 to 172 parts/trillion (lipid basis) (detection limit generally between 0.1 and 0.2 parts/trillion); two of the samples were composites of three samples and one was a composite of 4 samples(1). The 1,2,3,4,6,7,8-isomer was found in 2 samples of human breast milk collected in 1986 in Binghamton, NY, at concn of 1.26 and 1.74 parts/trillion (wet weight basis) and 44 and 60 parts/trillion (lipid basis)(1). The avg total concn in the fat fraction of human milk were 59.5 picogram/g in 4 samples from Sweden, 72.8 picogram/g in 5 samples from Germany, and 174 picogram/g in 1 sample from Denmark(2).
Pool samples of human milk collected in 1988 from Birmingham and Glasgow, UK, (40 mothers each city) contained 76 and 65 parts/trillion 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (fat basis), respectively(1). The concn found in a WHO/EURO Interlaboratory Comparison of a pooled 1987 sample of European human milk from a number of mothers and locations that were not specified contained 46 parts/trillion (fat basis)(1).
CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the transcription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (L177)
Tier 4 of the National Dioxin Study being conducted by the USEPA has analyzed for the presence of heptachlorodibenzo-p-dioxin in stack emissions and ash at 13 and 74 sites, respectively, throughout the U.S. representing many combustion source categories(1-3). Heptachlorodibenzo-p-dioxin has been detected in stack emissions from all of the 13 sites tested in Tier 4 at concn ranging from 0.22 to 5,900 ng/standard cu m of flue gas (normalized to 3% oxygen); the max level was detected in stack emissions from a secondary copper smelter(1,3). Some of the various ash samples were analyzed from all 74 sites in the Tier 4 study representing 22 combustion source categories did not contain detectable levels (detection levels varied; most were <1 ng/g)(2). The max concn found in ash were 2,340 and 478 ng/g in the settling chamber ash and bottom ash at a wire reclamation incinerator, 1012 ng/g in the ESP ash at a municipal solid waste incinerator, and 411 ng/g in the baghouse ash at a secondary copper smelter(2). The emissions found in studies similar to Tier 4 ranged from not detected to 1600 ng per standard cu m of flue gas, normalized to 3% oxygen) (detection limit not specified); the maximum emission rate was for a municipal waste combuster(3).
The amount of heptachlorodibenzo-p-dioxin found in 8 surface wipe tests at a multi-building site where it was presumed a polychlorobiphenyl transformer askarel was improperly disposed (in an incinerator in the immediate vicinity of the buildings) 12 years prior to the testing ranged from 39 to 4160 mg/sq m (avg 1,262 mg/sq m); the concn in 6 dust samples ranged from 24-2800 ng/g and averaged 865 ng/g(1). A concn of 900 ug/sq m was found in a second floor wipe test in an apartment building where a transformer fire had occurred in the basement(2). Average emission concn of 206 and 67 ng/cu m were detected in stacks from two municipal incinerators in Belgium which correspond to emission factors of 2.7 and 0.59 mg/ton of waste burned(3). A concn of >15,000 ppb was detected in oil leachates from a waste dump site in Germany which had been receiving waste oils and liquid chemical wastes; a concn of >25,000 parts/trillion was detected in sediments of a drain near the entrance to the municipal sewer and a concn of 93,000 parts/trillion was detected in sediments of a nearby stream which had received discharges from the dump until 1981 when the main drain was connected to the municipal sewer(4). Levels of 18-380 ng/cu m (normalized to 10% CO2) were detected in stack effluents from a municipal solid waste incinerator in Sweden in 1985(5).
The 1,2,3,4,6,7,9-isomer and 1,2,3,4,6,7,8-isomer of heptachlorodibenzo-p-dioxin were found at concn of 4.0 and 3.0, respectively, in soot samples from a 1981 PCB transformer fire in a Binghamton, NY, State Office Building(1). Heptachlorodibenzo-p-dioxin has been found at an avg concn of 6.0 ng/g in particulates taken from chimneys venting fireplaces burning untreated, residential wood supplies in several areas of the U.S.(2). The range of avg concn of heptachlorodibenzo-p-dioxin found in various effluent from three typical urban incinerators in Japan were 63-1120 ng/g in fly ash, 6.0-9.6 ng/g in bottom ash, and 22-1270 ng/g in sludge(3). 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin was detected in the automobile exhaust from 3 of 5 cars tested in a study in Australia at rates of emission ranging from 95-482 pg/km (avg 294 pg/km)(4). The total concn of heptachlorodibenzo-p-dioxin present in refuse samples at 2 Ontario, Canada, incinerators prior to incineration ranged from 2.0-19 and 20-87 ng/g, respectively; the avg concn were 8.8 and 45 ng/g(5).
The polychlorinated dibenzo-p-dioxins and the polychlorinated dibenzofurans are predominantly stored in fat, but they are also excreted in milk and pass the placenta. They also appear in the blood and vital organs at lower concentrations. /Polychlorinated dibenzo-p-dioxins/
A defined mixture of polychlorinated dibenzo-p-dioxins and dibenzofurans was subcutaneously administered to a pregnant marmoset monkey (Callithrix jacchus) 11 wk prior to delivery. Transfer of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans via placenta and mother's milk was investigated by measurement of concn in a newborn 1 day after birth and in an infant of the same litter after a lactation period of 33 days. Furthermore, comparative measurements were performed in different tissues of the mother at the end of the lactation period, and in addition, in two groups of four adult monkeys each 1 and 6 wk after treatment. Deposition of the polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans into fell liver was very low for most of the 2,3,7,8-substituted congeners. Highest deposition was observed for 2,3,7,8-tetrachlorodibenzo-p-dioxins and 1,2,3,7,8-pentachlorodibenzo-p-dioxins. For all other compounds concn in the hepatic tissue of newborn shortly after birth were lower than one tenth of corresponding concn in adults. Fetal liver isapparently largely unable to accumulate polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans. In contrast to liver, concn of 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans in adipose tissue of the newborn were at least one third of the levels in adults. However, concn of octachlorodibenzo-p-dioxin and octachlorodibenzofuran were about three times higher in the newborn than in adult adipose tissue. Transfer of some of the 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans to the offspring via mother's milk was considerable, leading to hepatic concn in the suckled infant at the end of the 33-day nursing period well above corresponding concn in the dam. When hepatic concn in the infant and dam were compared 2- to 4-fold higher concn were found in the infant's liver for 2,3,7,8-tetrachlorodibenzo-p-dioxins/furans and for 1,2,3,7,8-pentachlorodibenzo-p-dioxins. In the case of the 2,3,7,8-substituted hexachlorodibenzo-p-dioxins, hepatic concn in the infant and dam were in the same range at the end of the suckling period. In contrast to this, less than one tenth the concn of octachlorodibenzo-p-dioxin was found in the infant's liver when compared with adult liver. /Hexachlorodibenzo-p-dioxins/
The tissue distribution of 2,3,7,8-chlorine substituted dibenzo-p-dioxins was conducted in 11 patients who died of cancer. The concn of octachlorodibenzo-p-dioxin was the highest in each organ and tissue and heptachlorodibenzo-p-dioxins was also found at relatively high levels, second only to octachlorodibenzo-p-dioxin. The levels of 1,2,3,7,8-pentachlorodibenzo-p-dioxins and 1,2,3,6,7,8-hexachlorodibenzo-p-dioxins in the spleen were the highest, respectively. 2,3,7,8-Tetrachlorodibenzo-p-dioxins was also detected and its concn was the highest in the gonad (0.8-3.2 picogram/g range). From the 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalent calculations, the highest equivalent value was obtained from a 54-year old female who died of cancerous goiter. This individual had the highest concn of 2,3,7,8-substituted penta- and hexa-chlorodibenzo-p-dioxinss among the 11 patients. /Heptachlorodibenzo-p-dioxins/
For more Absorption, Distribution and Excretion (Complete) data for HEPTACHLORODIBENZO-P-DIOXIN (8 total), please visit the HSDB record page.
Contaminant of pentachlorophenol; [ChemIDplus]
Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (L177, L178)
One of the 21 tetrachlorophenol samples /that were analyzed/ contained ... 5.1 mg/kg ... /of/ heptachlorodibenzo-p-dioxin. ... Analysis /of 8 commercial pentachlorophenols/ ... showed ... heptachlorodibenzo-p-dioxins ... in the range of 0.5 to 39 mg/kg in 7 samples, and 3.3 to 15 mg/kg ... in 5 samples.
/Samples analyzed by mass fragmentography/ were found to contain ... 55 mg/kg of heptachlorodibenzo-p-dioxins /in commercial 2,3,4,6-tetrachlorophenol (TCP) and/ 235 mg/kg heptachlorodibenzo-p-dioxins /in technical pentachlorophenol (PCP)/. The positional isomers of the dioxins were not identified.
Heptachlorodibenzo-p-dioxins were found in both technical and analytical grades of commercial pentachlorophenol, as determined by gas chromatography coupled with several detection methods. When an electron capture detector was used, the technical grade product was found to contain 24 mg/kg ... and the analytical grade product had 0.04 mg/kg /of heptachlorodibenzo-p-dioxins/.
용도A toxic polychlorinated dibenzo-p-dioxin detected in domestic meat and poultry.
일반 설명Off-white powder. Insoluble in water.
Unidentified isomers of heptachlorodibenzo-p-dioxin were detected in chimney ash of a woodburning stove and fireplace at concn of 0.1 and 0.5 ppb, respectively; the concn in bottom ash samples ranged from 0.3 to 1.2 ppb in 2 different woodburning stoves and was 2.0 ppb in one fireplace(1). The bottom ash from an out-of-doors open-air burning device contained 11 ppb(1). The total concn of the 2 isomers of heptachlorodibenzo-p-dioxin in particulate samples centrifuged from effluent collected in Aug-Sept 1987 from 9 of 9 from Ontario, Canada, pulp and paper mills ranged from 7.7 to 430 parts/trillion (avg 104 parts/trillion); heptachlorodibenzo-p-dioxin was not detected in whole effluent samples collected from the same 9 plants in Nov 1987 (detection limits ranged from 0.01- 0.1 parts/trillion)(2). Emission rates from 4 resource recovery and incinerator facilities in Europe range from 158 to 3366 ug/ton municipal solid waste disposed (avg 1218 ug/ton; dates of sampling not specified); the emission rate in one U.S. facility was 37 ug/ton(3). Flue gas from test runs of a Swedish hazardous waste incinerator contained between 9.4 and 71 ng/cu m of total heptachlorodibenzo-p-dioxin(4).
The total emissions of heptachlorodibenzo-p-dioxin from a municipal incinerator in Florence, Italy, in Oct 1980, March 1982, and April 1985 were 100, 70, and 1400 ng/cu m of dry effluent in the condensate (organic vapors and very fine dust), respectively; the dust emission from the incinerator contained 56 and 3.0 ng/cu heptachlorodibenzo-p-dioxin in Oct 1980 and April 1985, respectively (total amounts of dust were 100 and 40 mg/cu m, respectively)(1). The concn of total heptachlorodibenzo-p-dioxin in fly ash collected from electrostatic precipitators from two municipal incinerators in 1981, one in the Midwest US and one on the East Coast, were 78 and 107 ng/g, respectively(2).